Wednesday, May 3, 2017

A middle-aged male called 911 for sudden severe chest pain. The medics were very worried about acute MI and recorded a prehospital ECG. It is unavailable, but looked like this:

As with many prehospital ECGs, the R-waves on top, & the S-waves on the bottom, are cut off.There is ST elevation in V2-V4. The medics were very worried about MI and asked to see me at the door to assess the ECG.What do you think?

I looked at it and immediately said: "This is LVH. Not MI." And so we did not place the patient in the critical care area and did not activate the cath lab.

What did I see? There is indeed ST elevation, but there is T-wave inversion also, and the TWI is in V4-V6. You might think it is Wellens', but Wellens' is a syndrome, not an ECG finding. It is a syndrome in which the pain has resolved (is gone). This patient's pain was still present.

Furthermore, a true Wellens' ECG has T-wave inversion in V2-V4, not just V4-V6. And it should not have high voltage. While Wellens' requires R-wave preservation in the affected leads, high voltage should make you think of what I call Pseudo-Wellens pattern due to LVH.

Here is a true Wellens' case, showing evolution over time, in a patient whose pain had resolved:

He was in severe pain and we were worried. He had a history of hypertension. We placed him in a room and recorded this ECG (this is actually the same one as above, but this time without cutting off the top and bottom.)

Classic LVH with ST-T abnormalities. Although this may hide a subtle myocardial infarction, it is a typical ECG for a patient with severe concentric LVH.

We did a point of care cardiac ultrasound and it showed LVH. We looked for, but did not see, a flap in the proximal aorta. The root was 4.1 cm in diameter (slightly large). We looked at the suprasternal notch but could not get a good view. The abdominal aorta did not show a flap.

A troponin I returned elevated at 0.115 ng/mL. So this is diagnostic of myocardial injury, and probably of MI, but not necessarily of ACS! We have done many studies in our department of Type I and Type II MI (see references below) and most patients in our ED with elevated troponin either do not have MI (myocardial injury from etiologies other than ischemia) or have Type 2 MI (due to ischemia but not due to ACS).

A D dimer returned at 13,000 (very high!). This is a good screening test for aortic dissection and normal for our assay is less than 230.

In spite of chronic renal insufficiency (Cr = 4 mg/dL), we sent him for an aortic CT:

Without all the images, it may be difficult to see, but this was an acute dissection from the aortic root all the way to the iliac arteries.

It is important to recognize Pseudo-infarction patterns not just because it prevents unnecessary cath lab activation, but because if you don't recognize it, you will have diagnostic momentum towards the wrong diagnosis (ACS) and away from the correct diagnosis (in this case, aortic dissection).

Instructive case with important messages! As to the ECG — features supporting a non-acute picture are: i) How extreme the increase in voltage is (through the overlap in V4-V5, one can see that the R in V5 is no less than 31mm! — and the S in V2 no less than 25mm! — not too mention the S in V3 that goes off the page); ii) If one flips this ECG upside down (ie, applies the “mirror test”) — the slightly elevated ST-T waves seen in V1,V2,V3 now take on an appearance identical to that expected for lateral lead LV “strain”; and iii) The “pseudo-Wellens” ST-T wave appearance that we see in lead V4 is exactly what one might expect if you “fused” the ST-T wave appearance in neighboring leads V3 and V5. I generally write down on my official interpretation, “LVH with strain and/or ischemia” for my assessment of ST-T wave appearance seen here in the 6 chest leads — but the important point, is to appreciate how this overall ST-T wave pattern is probably longterm, and clearly unlikely to account for this patient’s acute and very worrisome symptoms. THANKS to Dr. Smith for posting this case!

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